interactionist approach to sz

the diathesis-stress model

- research shows the importance of bio and environmental factors in sz

- an explanation that links biological vulnerability to environmental stressor

- this model explains that individuals will develop sz if they have a biological predisposition and if they are exposed to stressful situations

Diathesis = a predisposition to develop a medical condition 

Stress = any environmental factor that  

AO3 - strength of interactionist approach to sz: supporting evidence: Tienari et al. (2004) 

procedure: hospital records were reviewed for nearly 20,000 women admitted to Finnish psychiatric hospitals between 1960-79, identifying those that had been diagnosed at least once with sz

- the list was checked to find mothers who had 1+ of their offspring adopted away. the resulting sample of 145 adopted-away offspring (the high-risk group) was matched with a sample of 158 adoptees without this genetic risk (low risk group)

- both groups of adoptees were independently assessed after an interval of 12yrs, with a follow up after 21yrs

- psychiatrists also assessed family functioning in the adoptive families using the Oulu Family Rating Scale (OPAS scale). it measures families on various aspects of functioning such as parent-offspring conflict, lack of empathy and insecurity

- the interviewing psychiatrists were kept blind as to whether the biological mother was schizophrenic or not

findings: of the 303 adoptees, 14 developed sz over the course of the study

- 11 of these were from the high-risk group and 3 from the low-risk group

- however, being reared in a ‘healthy’ adoptive family appeared to have a protective effect even for those that had a high genetic risk

- in adoptees at high risk of sz, but not in those at low genetic risk adoptive-family stress was a significant predictor of the development of sz

AO3: strength of interactionist approach to sz: real world application

- the combination of drug treatments enhances their effectiveness

- e.g. Tarrier et al. (2004) randomly allocated 315 pps to (1) medication + CBT, (2) medication + counselling, or (3) control group (medication only)

- pps in the two combination groups showed lower symptoms following the trial than the medication-only group, though there was no difference in hospital readmission.  

- this means that there’s a clear practical advantage to adopting an interactionist approach to sz in terms of superior treatment outcomes

Meehl’s (1962) original diathesis-stress model 

- diathesis (vulnerability) is entirely genetic – the result of a single schizogene, which led to a biologically based schizotypic personality – extremely sensitive to stress

- no amount of stress will lead to sz if the gene is not present 

- however, chronic stress in someone with the gene could lead to the development of the disorder – nature and nurture interact

modern understanding of diathesis

- Ripke et al. (2014) - many genes each appear to increase genetically vulnerability only slightly, there’s no single ‘schizogene’

- modern views of diathesis also include a range of factors beyond the genetic, including psychological trauma (Ingram and Luxton, 2005) - so trauma becomes the diathesis rather than the stressor

- Read et al. (2001) proposed a neurodevelopmental model in which early trauma alters the developing brain. early and severe enough trauma, such as child abuse, can seriously affect many aspects of brain development. e.g. the hypothalamic-pituitary-adrenal (HPA) system can become overactive, making a person much more vulnerable to later stress.

modern understanding of stress

- in the og diathesis-stress model of sz, stress was seen as psychological in nature, in particular related to parenting

- although psychological stress, including that resulting from parenting may still be considered important, a modern definition of stress (in relation to the diathesis-stress model) includes anything that risks triggering sz (Houston et al. 2008)

- much of the recent research into factors triggering an episode of sz has concerned cannabis use. in terms of the diathesis-stress model cannabis is a stressor because it increases the risk of sz by up to 7x according to dose. this may be because cannabis interferes the dopamine system. however, most people do not develop sz after smoking cannabis presumably because they lack the requisite vulnerability factors. 

treating according to the interactionist model

- compatible with both bio and psych treatments. in particular the model is associated with combining antipsychotic medication and psychological therapies, most commonly CBT

- Turkington et al. (2006) point out that it’s possible to believe in bio causes of sz and still practice CBT to relieve psych symptoms. however, this requires adopting an interactionist model – it’s not possible to adopt a purely bio approach and tell schizophrenics that their condition is purely bio and that there’s no psych significance to symptoms, and then to simultaneously treat them with CBT. 

AO3 - limitation of treating according to the interactionist model

treatment-causation fallacy: 

- if excess dopamine isn’t the cause of sz but treating the disorder with drugs, then we’re not treating the underlying root cause, may just be suppressing the symptoms

- the same could be said for psych treatments, if the roots of sz aren’t in the mind or the family but treating those aspects, then the underlying actual cause isn’t being dealt with.